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Heme Oxygenase-mediated Resistance to Oxygen Toxicity in Hamster Fibroblasts
Journal article   Open access   Peer reviewed

Heme Oxygenase-mediated Resistance to Oxygen Toxicity in Hamster Fibroblasts

Phyllis A. Dennery, Kunju J. Sridhar, Christen S. Lee, Hubert E. Wong, Vida Shokoohi, Pamela A. Rodgers and Douglas R. Spitz
The Journal of biological chemistry, Vol.272(23), pp.14937-14942
06/1997
DOI: 10.1074/jbc.272.23.14937
PMID: 9169465
url
https://doi.org/10.1074/jbc.272.23.14937View
Published (Version of record) Open Access

Abstract

The role of heme oxygenase (HO)-1 was evaluated in the oxygen-resistant hamster fibroblast cell line, O2R95, which moderately overexpress HO when compared with the parental cell line, HA-1. To suppress HO-1 expression, O2R95 were transfected with HO-1 antisense oligonucleotide or treated with tin-mesoporphyrin (SnMP). To increase HO-1 expression, cells were transfected with HO-1 cDNA in a pRC/cytomegalovirus (CMV) vector. All cells were challenged with a 48-h exposure to 95% O2 (hyperoxia). When HO activity was suppressed, O2R95 cells had significantly decreased cell viability, increased susceptibility to lipid peroxidation, and increased protein oxidation in hyperoxia. In contrast, further overexpression of HO-1 did not improve resistance to oxygen toxicity. Antisense-transfected cells and SnMP-treated cells with lowered HO activity showed increased levels of cellular heme compared with controls. In the HO-1 cDNA-transfected O2R95 cells, cellular heme was lowered compared with controls; however, cellular redox active iron levels were increased. We conclude that HO mediates cytoprotection to oxygen toxicity within a narrow range of expression. We speculate that this protective effect may be mediated in part through increased metabolism of the pro-oxidant heme but that higher levels of HO activity obviate protection by increased redox active iron release.

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